ABSTRACT
This chapter explores what is known about the pathophysiology of carbon monoxide (CO) poisoning and the development of both biochemical and anatomic lesions in light of our present knowledge. Mild poisoning produces no measurable long-term aftereffects, but as the severity of the exposure increases, the likelihood of developing mild to severe neurologic sequelae increases, assuming the patient survives. If the patient has attempted suicide, the organic brain syndrome following poisoning may be misinterpreted as depression. M. Olsky and J. R. Woods, in reviewing 100 consecutive CO poisonings admitted to Lutheran General Hospital in Park Ridge, IL, also found that admission carboxyhemoglobin levels bore no statistical relationship to outcome. The question arises as to what the ultimate mechanism is for damage to brain tissues following CO poisoning. It is clear that hypoxia plays a central role, as demonstrated by most investigators.
